Increased ICP and
Herniation Syndrome
Gerald Pagaling
Objectives
 Discuss the mechanisms for the homeostasis of ICP.
 Enumerate the different types of Herniation
Syndromes.
 Discuss the appropriate management in increased
ICP.
Monroe Kellie Doctrine
….The intact cranium and vertebral canal, together
with the relatively inelastic dura , form a rigid
container, such that an increase in the volume of any
of its contents – (Brain, Blood or CSF) – will elevate
the ICP. Furthermore, and increase in any one of
these components must be at the expense of the
other two…
0%
9%
4%
Brain Tissue
CSF
Blood Vessel
87%
Meninges
Corollary
The restrictions apply to each
compartment (R vs L supratentorial
space, infratentorial space, spinal
subarachnoid space.
A. Buffering effect of displacement of CSF from
the cranial cavity to the spine.
B. Stretching of the infoldings of the relatively
unyielding dura (Falx Cerebri).
C. Slow formation of CSF during raised ICP
D. Brain deformation.
Intracranial Elastance
25 mmHg
Cerebral Perfusion Pressure
CPP : MAP - ICP
Normotensive: 10-15mmHg
Diminished CBF: 40-50mmHg
Therapeutic Target: <15-20mmHg
SSP Handbook of Stroke
ICP: 5 -10 mmHg
CP: 70-100 mmHg
Interstitial Edema
Noncommunicating Hydrocephalus:
 Movement of Sodium and Water across the ventricular wall
and paraventricular space.
Clinical Presentation
Direct
Bilateral
Papilledema*
Headache
Brain
Dysfunction
Vomiting
Indirect
Decrease in
Sensorium
Pupillary Dilatation
Abducens Palsy
Cushing Response
A. Papilledema
The optic nerve is surrounded by dural and
subarachnoid sleeve, which contains CSF
that communicates with the CSF in the
subarachnoid space
Retinal Veins
 ICP rise dampens the venous pulsations.
 With obstruction, retinal veins becomes larger and
more numerous
The presence of
retinal venous
pulsations is a good
but not invariable sign
of normal ICP
Engorgement of
retinal veins is a
reliable early
sign of ICP
 Impaired Axoplasmic Flow – enlargement of Blind
Spot
 Failure of Ganglion Cells – Concentric Vision Loss
B. Headache
Subtle distortions of pain receptors in
cerebral blood vessels and meninges.
Venous Obstruction
C. Cushing’s/Vasopressor Response
Hypertension
 Induction of CNS Ischemic response due to CSF
Pressure>Arterial Pressure.
Bradycardia
Stimulation of Vagus Nerve due to rise in
Arterial Blood Pressure via the Baroreceptors
in Aortic Arch
Irregular Respiration
Increased ICP
Herniation Syndromes
Dislocation of a portion of the cerebral or cerebellar
hemisphere from its normal position to an adjacent
compartment that is bounded by dural folds, a phenomenon that
is evident both at the autopsy table and by imaging of the brain.
Major Patterns of Brain Shift
Supratentorial
Falcine Herniation
Lateral displacement of
the diencephalon
Uncal Herniation
Central Transtentorial
Herniation
Rostrocaudal Brainstem
Herniation
Infratentorial
• Tonsillar Herniation
• Upward Brainstem
Herniation
Supratentorial Herniation
1. Falcine
Displacement of the cingulate gyrus under the
falx.
ACA: Pericallosal & Callosomarginal branches
2. Lateral Displacement of
Diencephalon
Roughly correlated
with impairment of
consciousness
0-3mm: Alert
3-5mm: Drowsy
6-8mm: Stupor
9-13mm: Coma
3. Uncal/Lateral Transtentorial
Uncus/Medial edge
of temporal lobe
herniates
medially
and downward over
the free tentorial
edge
into
the
tentorial notch.
3. Uncal/Lateral Transtentorial
1. Ipsilateral Fixed and
Dilated Pupil:
2. Impaired
Consciousness:
passing through the
midbrain and adjacent
diencephalon.*
3. Uncal/Lateral
Transtentorial
3. Contralateral/Ipsilateral Hemiparesis - CST
4. Visual Field Defect. - PCA
Stages
1. Early Third Nerve
2. Late Third Nerve
3. Midbrain Upper Pontine
Early
Third
Nerve
Late
Third
Nerve
-Rapid Lapse into
coma.
-Kernohan’s
Notch
-Hutchinson Pupil
(Dilated
Nonreactive
Pupil)
Midbrain
Upper
Pontine
4. Central Transtentorial
Medial
 Pressure on the
Diencephalon.
(Small penetrating
endarteries)
Dorsal/Parinaud
Stages
1.
2.
3.
4.
5.
Early Diencephalic Stage
Late Diencephalic Stage
Midbrain Stage
Pontine
Medullary/Terminal
Early Diencephalic
-Changes in alertness and behavior
-Warns of a potential reversible lesion that is about
to encroach the brainstem creating a irreversible
damage.
-Similarity with Metabolic Encephalopathy.*
Early
Diencephalic
Ciliospinal Reflex.
Late Diencephalic
More distinct clinical appearance:
 More difficult to arouse.
 Decorticate Posturing
Late
Diencephalic
Midbrain
-Oculomotor Dysfunction
-Heightened Motor and Tendon Reflexes
Midbrain
Upper
Pontine
Pontine
-Shallow and Irregular Breathing.
-Flaccid motor tone.
Pontine
Medulla
-Irregular and Slow Breathing
-No Chance of Useful recovery
-Terminal Stage
Dorsal Midbrain
Usually caused by pathology of the Pineal
gland or Posterior Hypothalamus
Impairment of consciousness
Dilated Pupil
Upward gaze palsy
Convergence Weakness
Convergence-Retraction Nystagmus
Eyelid Retraction (Collier Sign)
Dorsal
Midbrain
Dorsal Midbrain
Usually caused by pathology of the Pineal gland or
Posterior Hypothalamus
Upward gaze palsy
Sundowning
Deficit of convergent eye movements
Retractory Nystagmus
Eyelid Retraction
Rostrocaudal Deterioration
Downward
displacement
of
midbrain or pons
Paramedian Ischemia (Duret
Hemorrhage):
Stretching
of
perforating branches of basilar
artery
Infratentorial Herniation
Tonsillar Herniation
Impact
of
cerebellar
tonsils across
the
foramen
magnum
impinging the
caudal
medulla
Tonsillar Herniation
Sudden cessation of breathing.
Rapid increase in blood pressure.
Also seen in patient who had undergone
lumbar puncture with intracranial mass.
Upward Brainstem Herniation
Superior surface of the cerebellar vermis
and midbrain are pushed upward,
compressing the dorsal mesencephalon,
adjacent blood vessels and cerebral
aquedect.
Respiratory
disturbance,
cardiac
irregularity, loss of consciousness
Upward Brainstem Herniation
Decerebrate posturing and pupillary
changes-initially both pupils are miotic but
still reactive, progressing to anisocoria and
enlargement-to this type of brain
displacement.
Compression of SCA
Management
GOAL
ICP: <20mmHg
CPP: >50mmHg
Medical Management
General Measures
Control Agitation and pain with NSAIDs and
Opioids
Avoid Hyperthermia
Seizure Control
 Phenytoin LD: 18-20 MKD MD:3-5MKD
 Levetiracetam: 500mg IV q12
General Measures
 Stool Softeners: Lactulose 30cc OD HS
 Maintenance of Normal Fluid and Electrolyte
Imbalance
 Avoid excessive free water/hypotonic solution
 Normal Volume Status (3-3.5liters per day in 60kg)
 Hyperosmolar state
A. Head at Midline with HOB
Elevated (30–45°)
Reducing ICP without affecting MAP*
Raises the differential between MAP
and CPP.
B. Hyperventilation
Most rapid but temporary (20-40 min) technique
for lowering ICP
Respiratory Alkalosis (PaCo2: 25-30mmHg vs 3035mmHg) leading to Cerebral vasoconstriction*
C. Intubate
Most rapid but temporary (20-40 min) technique
for lowering ICP
Respiratory Alkalosis (PaCo2: 25-30mmHg vs 3035mmHg) leading to Cerebral vasoconstriction*
D. Hyperosmolar Therapy
 is the creation of a gradient of water concentration
from the brain to the blood that reduces brain
volume.
Serum
Hyperosmolarity
Diuresis
Hypernatremia
and
Hypovolemia
D. Hyperosmolar Therapy
Mannitol
Hypertonic Saline
Dexamethasone
D. Mannitol
20% Solution (1.5 – 2g/kg by bolus
Injection)
Benefits
Risks
-Lowers Blood Viscosity -Renal Failure
-Increases Cerebral
Perfusion
-Free Radical Scavenger
D. Hypertonic Saline
• Continuous 3% NaCl infusion at a rate of 1050mL/hr and titrated q2hours per sliding
scale.
• Target Serum Sodium: <160mmol/L
D. Hypertonic Saline
D. Hypertonic Saline
D. Hypertonic Saline
D. Hypertonic Saline
D. Hypertonic Saline
D. Hypertonic Saline
HTS Protocol:
Benefits
Risks
-Comparable with Mannitol
-Serial Serum Sodium Monitoring
D. High Dose Dexamethasone
Loading Dose: 10-100mg IV bolus
Maintenance Dose: 4 – 24mg IV q6
Decreases transfer of substance on a disrupted
BBB.
Benefits
Risks
-Improved compliance of brain
tissue
-Diminish Plateau waves
-Bacterial Meningitis (10mg q6)
-Not applicable for vascular
hemorrhage/infarction.
-Contraindicarted in head Injury
-Hyperglycemia*
D. Pentobarbital
Loading Dose: 10mg/kg over 30 minutes
followed by 5mg/kg for 60 minutes x 3 doses
Maintenance Dose: 1-3mg/kg to maintaine
plasma concentration of 3-4mg/dL.
Same with Propofol and Midazolam
Benefits
Risks
-ICP decreases rapidly and
usually remains low as long as
the patient is anesthetized
-The effect of this treatment on
long-term outcome is not dramatic
and the frequent monitoring of
EEG, drug levels, and potential
cardiopulmonary complications
make it extremely labor intensive.
- Requires an ICU Set-up
ICP Monitoring
Patients with GCS less than or equal to 8m
significant IVH NS Hydrocephalus
Maintaining CPP: 60-70mmHg
Different Types:
 Intraventricular*
 Intraparenchymal
 Subarachnoid Screw bolt
 Subdural
 Epidural
Surgical Management
Decompressive Hemicraniectomy with
Duraplasty.
Bone Flap: 12x9cm
Removal of Bone Flap: 15% decrease
Opening of the Dura: 70% decrease
Thank you
Sources:
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10th edition. 2014. 978-0-07-180091-4
 Posner, et. Al. Pluma and Posner’s Diagnosis of Stupor and
Coma 4th Edition. 2007. 978-0-19-532131-9
 Biller, et. Al. De Myer’s The Neurlogic Examination A
Programmed Text 6th Edition. 2011. 978-0-07-170117-4
 Greenberg, M.S. Handbook of Neurosurgery 8th Edition.
2016. 9781626232426
 Guyton and Hall. Textbook of Medical Physiology 11th Edition.
2006. 0-7216-0240-1